In man, cirrhosis with portosystemic shunting as a consequence of portal hypertension produces changes of systemic circulation, i.e. hyperdynamic circulatory syndrome, which are characterized by decreased peripheral vascular resistance as well as increased cardiac output, systolic ejection rate, and intrapulmonary venous admixture [4, 11, 12]. In addition, changes of renal perfusion, i.e., hyperperfusion of the medulla with diminished perfusion of the cortex, have been demonstrated. Functional renal failure as a consequence of decompensated cirrhosis (i.e., so-called hepatorenal syndrome) have been partially attributed to these intrarenal perfusion changes [8].
